Key result
Labetalol blocked stress-induced increases in free fatty acids and lowered triglycerides, whereas elevations in total, HDL, and LDL cholesterol were caused by accompanying hemoconcentration.
Why the study?
Does labetalol alter serum lipid and hemoconcentration responses to brief mental stress in healthy males?
RCT (n=52)
2x2 factorial
Does labetalol alter serum lipid and hemoconcentration responses to brief mental stress in healthy males?
Elevations in total, HDL, and LDL cholesterol during acute mental stress are driven by hemoconcentration, whereas increases in free fatty acids and triglycerides are mediated by sympathetic activation.
Answers are grounded in this paper and cite their sources.
Labetalol attenuates sympathetic-driven FFA/triglyceride rises during stress; confirms hemoconcentration as the driver of acute cholesterol elevations.
Objective Previous studies suggest that hemoconcentration may be one mechanism by which acute psychological stress causes elevations of serum total cholesterol and its subfractions. Alternatively, such elevations may result from sympathetically mediated changes in lipid metabolism. This study evaluated these two hypotheses by manipulation of sympathetically mediated responses to stress using a nonselective adrenoceptor antagonist, labetalol. Method In a 2 × 2 factorial design, 52 healthy male participants were randomly assigned to a stress or no-stress condition and, within each condition, were administered either labetalol or saline. Participants assigned to stress completed three cognitive and evaluative tasks lasting a total of 18 minutes. Indices of hemoconcentration (hematocrit and hemoglobin), heart rate, blood pressure, and serum lipids (total, high-density lipoprotein (HDL), low-density lipoprotein (LDL), free fatty acids, and triglycerides) were assessed at preinfusion and infusion baselines and after mental stress (or rest). Results Labetalol reduced sympathetic activation, as shown by a substantial reduction in heart rate elevation during stress, but did not alter changes in blood pressure or in hemoconcentration, as indicated by equivalent increases in hematocrit and hemoglobin in the two stressed groups. Labetalol blocked stress-induced increases in free fatty acid concentrations and lowered triglyceride levels but did not influence rises in total, HDL, or LDL cholesterol among stressed subjects. However, arithmetic correction for hemoconcentration eliminated the increases in total, HDL, and LDL cholesterol. Conclusions These findings suggest that elevations in total cholesterol and its HDL and LDL subfractions during acute stress are caused by accompanying hemoconcentration, whereas concomitant rises in free fatty acids and triglycerides result from the direct metabolic effects of sympathetic activation.
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Bachen et al. (2002) conducted an RCT in Healthy (n=52). Labetalol vs. Saline was evaluated on Indices of hemoconcentration, heart rate, blood pressure, and serum lipids. Labetalol blocked stress-induced increases in free fatty acids and lowered triglycerides, whereas elevations in total, HDL, and LDL cholesterol were caused by accompanying hemoconcentration.
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